ArticleMolecular and cellular biochemistry2012
The hypoxic preconditioning agent deferoxamine induces poly(ADP-ribose) polymerase-1-dependent inhibition of the mitochondrial respiratory chain.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Low-dose intranasal deferoxamine modulates memory, neuroinflammation, and the neuronal transcriptome in the streptozotocin rodent model of Alzheimer's disease.Frontiers in neuroscience · 2024Article
- Deferoxamine accelerates endothelial progenitor cell senescence and compromises angiogenesis.Aging · 2021Article
- Review
- Regulation of HFE expression by poly(ADP-ribose) polymerase-1 (PARP1) through an inverted repeat DNA sequence in the distal promoter.Biochimica et biophysica acta · 2013Article
- Deferoxamine: emerging, new neuro-protective benefits.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2013Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
We previously reported that treatment with a single dose of deferoxamine (DFO), which acts as a hypoxic-mimetic agent, only induces reactive oxygen species (ROS) production in the presence of poly(ADP-ribose) polymerase (PARP-1). Given that mitochondria are one of the main sources of ROS, the present study was designed to assess the effect of DFO treatment on the activity of mitochondrial respiratory chain complexes, and more importantly, to determine whether this effect is modulated by PARP-1. We found that DFO treatment induced a progressive decline in complex II and IV activity, but that this activity was preserved in PARP-1 knock-out cells, demonstrating that this decrease is mediated by PARP-1. We also confirmed that complex II inhibition after DFO treatment occurs in parallel with poly-ADP ribosylation. Consequently, we recommend that PARP-1 activation be taken into account when using DFO as a hypoxia-mimetic agent, because it mediates alteration of the mitochondrial respiratory chain.
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